Evidence map›Paper›PMID 28869603›Full record

ArticleOncogene2017

A regulatory circuit composed of DNA methyltransferases and receptor tyrosine kinases controls lung cancer cell aggressiveness.

F Yan, N Shen, J Pang, N Zhao, B Deng, B Li, Y Yang, P Yang, J R Molina, S Liu

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. DNA methylation in pulmonary fibrosis and lung cancer.Expert review of respiratory medicine · 2022
    Review
  4. Article
  5. Article
  6. An Assessment on Ethanol-Blended Gasoline/Diesel Fuels on Cancer Risk and Mortality.International journal of environmental research and public health · 2021
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. A dynamic NCell research · 2018
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

F YanThe Hormel Institute, University of Minnesota, Austin, MN, USA.
N ShenThe Hormel Institute, University of Minnesota, Austin, MN, USA.
J PangThe Hormel Institute, University of Minnesota, Austin, MN, USA.
N ZhaoThe Hormel Institute, University of Minnesota, Austin, MN, USA.
B DengDivision of Epidemiology, Mayo Clinic, Rochester, MN, USA.
B LiDepartment of Microbiology and Immunology, University of Louisville, Louisville, KY, USA.ORCID 0000-0001-5363-7070
Y YangDivision of Epidemiology, Mayo Clinic, Rochester, MN, USA.
P YangDivision of Epidemiology, Mayo Clinic, Rochester, MN, USA.
J R MolinaDepartment of Medical Oncology, Mayo Clinic, Rochester, MN, USA.
S LiuThe Hormel Institute, University of Minnesota, Austin, MN, USA.
University of Minnesota · USMayo Clinic in Arizona · USUniversity of Louisville · US

Funding

Targeting aberrant epigenetics by nanomedicineR01CA149623 · NCI · UNIVERSITY OF MINNESOTA · PI LIU, SHUJUN · 2010 to 2014
$1.8M
Bioactive compound modulation of epigenetic regulator Sp1/NFkB/miR network in AMLR21CA155915 · NCI · UNIVERSITY OF MINNESOTA · PI LIU, SHUJUN · 2011 to 2012
$365k
NCI NIH HHS R01 CA149623NCI NIH HHS R21 CA155915
6 · The paper itself

Abstract

Overexpression of DNMT1 and KIT is prevalent in lung cancer, yet the underlying molecular mechanisms are poorly understood. While the deregulated activation of DNMT1 or KIT has been implicated in lung cancer pathogenesis, whether and how DNMT1 and KIT orchestrate lung tumorigenesis are unclear. Here, using human lung cancer tissue microarrays and fresh frozen tissues, we found that the overexpression of DNMT1 is positively correlated with the upregulation of KIT in tumor tissues. We demonstrated that DNMT1 and KIT form a positive regulatory loop, in which ectopic DNMT1 expression increases, whereas targeted DNMT1 depletion abrogates KIT signaling cascade through Sp1/miR-29b network. Conversely, an increase of KIT levels augments, but a reduction of KIT expression ablates DNMT1 transcription by STAT3 pathway leading to in-parallel modification of the DNA methylation profiles. We provided evidence that KIT inactivation induces global DNA hypomethylation, restores the expression of tumor suppressor p15

Indexed as

AnimalsCell Line, TumorDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationHumansLung NeoplasmsMaleMiceMice, Inbred C57BLMicroRNAsProto-Oncogene Proteins c-kitSp1 Transcription FactorTumor Suppressor Protein p53DNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanMicroRNAsMIRN29a microRNA, humanProto-Oncogene Proteins c-kitSP1 protein, humanSp1 Transcription FactorTumor Suppressor Protein p53

Identifiers

PMID28869603
PMCPMC5730463
OpenAlexW2752723294

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.